A Novel Ruthenium-Fluvastatin Complex Downregulates SNCG Expression to Modulate Breast Carcinoma Cell Proliferation and Apoptosis via Activating the PI3K/Akt/mTOR/VEGF/MMP9 Pathway

Figure 12

(a) Histological appearance of mammary tissue of normal control showing the terminal duct lobular units (td), alveoli (a), alveolar septa (sg), acinus (ac), and serous gland (sg). (b) DMBA control shows atrophy of glands with periductal stromal fibrosis and fatty tissue (psf), atrophy of glands (ag) with surrounding fatty tissue, atrophy of serous glands (asg) with surrounding stromal fibrosis, and atypical hyperplasia (ah). (c) Mammary tissue of the DMBA-induced group treated with 25 mg/kg ruthenium-fluvastatin complex showing atrophy of serous glands (asg), atrophy of glands (ag), and periductal stromal fibrosis and fatty tissue (psf). (d) Mammary tissue of the DMBA-induced group treated with 50 mg/kg ruthenium-fluvastatin complex showing hyperplasia of serous and mucinous glands (h). (e) Mammary tissue of the DMBA-induced group treated with 75 mg/kg ruthenium-fluvastatin complex having almost normal architecture. (f) Mammary tissue of the DMBA-induced group treated with 50 mg/kg ruthenium. (g) Mammary tissue of the DMBA-induced group treated with 50 mg/kg fluvastatin. (h) Effect of the ruthenium-fluvastatin complex on in vivo antioxidant enzymes: SOD (superoxide dismutase), CAT (catalase), and GST (glutathione). as compared to the carcinogen control; ^# as compared to the ruthenium, fluvastatin, and ruthenium-fluvastatin (25, 50, and 100 mg/kg).

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